LAM2.14: Ruminant Neuro Part 3 - Toxic Dzs of the Brain

Locoweed Intoxication etiology

Oxytropis or Astragalus plants - among first green plants in the spring and proliferate in areas of overgrazing.

Toxic principles of Locoweed intoxication (3)

Selenium accumulation.

Teratogenic.

Interfere w/ alpha-mannosidase activity - leading to LSD.

Livestock normally shun locoweed

due to its bitter taste, but can become habituated to it

Age normally affected by locoweed intoxication

weaned calves as they are transitioning to grasses (bad baby moos)

After several weeks of ingestion of locoweed, there is

vacuolation in the cells that begins to affect their fxn.

CS of Locoweed Intoxication (6)

Loco - behavior changes (aka bad baby moos).

ataxia.

CP deficits.

Poor growth.

Abortion/malformation.

High altitude dz.

CP findings w/ locoweed intoxication

Vacuolated lymphocytes in blood/CSF.

Tx for Locoweed Intoxication

None, other than removal from source.

Calves severely affected by Locoweed intoxication will be

poo-doers, hope they grow out of it.

Lesions of Locoweed Intoxication

Microscopic vacuolation of neurons, lymphocytes, and renal tubular cells (alpha mannoside)

Nervous toxicosis is though to be due to a

labile neurotoxin secreted by Eimeria in the GIT.

Which parasites can directly colonize the CNS

Neospora and Sarcocystic

Nervous Coccidiosis CS (7)

Normal coccidiosis signs - D, tenesmus, and hetamtochezia.

Ataxia.

Tremors.

Opisthotonus.

Nystagmus.

Vocalization.

Seizure/coma.

CP findings of Nervous Coccidiosis may include

electrolyte loss w/ D.

Dx of Nervous Coccidiosis

just ID the coccidia - presumptive

Tx for Nervous coccidiosis (3)

Thiamine.

Tx for coccidiosis.

Ca-Mg cmpds - concurrently txs transport tetany.

Top Ddx for Nervous Coccidiosis

BVDV.

Water/Salt Intoxication occurs when animals are (2)

water deprived for an extended period then allowed to drink a lot.

Fed a high salt diet w/ insufficient or no H2O avaiable (then possibly allowed to drink a lot).

Regardless of circumstances, the pathophys of Water/Salt Intoxication (prior to reintroduction of H2O) (3)

an increase in plasma Na+ leads to initial brain dehydration.

Production of idiogenic osmoles in the brain (takes time).

CNS/CSF Na increase to maintain fluid equilibrium.

Pathophys of Water/Salt Intoxication once H2O is reintroduced

a rapid drop in plasma Na+ and fluid shifts into the brain, causing intracranial edema and increasing ICP.

Epidemiology of Water/Salt Intoxication (4)

Increased risk in animals fed >4% salt or water deprived.

Transport.

Shows.

broken pumps forcing water restriction.

Which animals can tolerate higher salt concentrations

those allowed free access to H2O.

CS of Water/Salt Intoxication (3, last w/ 4ex)

GI irritation from (large volume) H2O absorption can lead to D.

IV hemolysis leading to hemoglobinemia and hemoglobinuria.

Polio signs - ataxia, blindness, seizures, head-pressing.

CP findings for Water/Salt Intoxication (2)

Compare plasma to CSF Na+. CSF should normally be slightly lower than plasma.

Evidence of IV hemolysis.

CSF finding indicative of Water/Salt Intoxication

CSF Na+ > 160 mEq/L.

Dx of Water/Salt Intoxication (3)

CS.

HX.

CP.

Water/Salt Intoxication Tx

Slowly restore brain fluid and Na balance - too rapid will lead to brain overhydration or dehydration.

Use isotonic or mildly hypertonic fluids (Na conc similar to blood) IV plus hypotonic PO fluids

Why might you avoid hypotonic fluids w/ Water/Salt Intoxication

they promote water shifts into the braon.

Drugs to consider w/ Water/Salt Intoxication to reduce edema

Steroids or mannitol.

Lesions of Water/Salt Intoxication (2)

Cerebral edema w/ cortical necrosis.

possible eosinophilic perivascular cuffing.

Enterotoxemia Etiology

Overgrowth of C. perf type D - secretion of Epsilon toxin.

C perf type D is more likely to proliferate w/

high carb/energy diet.

Enterotoxemia is a dz of

sheep, but can see on cattle and goats

Epsilon toxin leads to (2)

increased gut permeability, enhancing its own absorption (and that of other toxins).

increased vascular permeability.

Degeneration of the vascular endothelium from epsilon toxin w/ Enterotoxemia leads to

Foci of necrosis in the brain which are more pronounce in sheep than goats.

Dz course of Enterotoxemia

Short. Often young animals (older than neonates) are found dead w/o previous known abnormalities.

Signs of neuro form of Enterotoxemia (3)

Staggering.

Clonic convulsions.

Opisthotonus.

CP findings for Enterotoxemia (3)

Neutrophilic leukocytosis.

Hyperfibrinogenemia if they live long enough.

Hyperglycemia and glucosuria (due to shock).

Tx for Enterotoxemia (3)

Supportive.

ABX - penicillin at 2x dose.

Anti-toxin.

Necropsy findings of Enterotoxemia

Blood-tinged fluid in body cavities.

Focal Symmetric Encephalomalacia may occur in conjunction w/

outbreaks of enterotoxemia - sublethal doses of epsilon toxin may lead to chronic neuro dz in sheeps of all age, and rarely in calves/goats.

Risk factors for FSE in addition to normal Enterotoxemia risk factors include (3)

moving to new pasture.

grazing young, green cereal crop pastures.

Anti-helminthic admin 1-2wks prior.

Postulated etiology of FSE in pigs (and possibly camelids)

subacute selenium toxicosis.

Clinical findings w/ FSE (4)

Dummy syndrome - aimless wandering.

Central blindness.

Incoordination.

Bilateral CN signs - jaw drop and inability to swallow.

Necropsy findings w/ FSE

Gross and microscopic hemorrhage and FSE.

FSE affects what portion of the brain more than polio?

White matter and brainstem.

Tx for FSE

Supportive - ultimately 90% fatality (you cannot fix holes in the brain).

Prevention of FSE

Vxn, but dz can occur in well vxn sheep.

Ammonia or urea are added to

poor quality feed to enhance digestibility (also reduce endophyte toxin)

In excess (>3% Dm), ruminal ammonia production will

outstrip AA production, and excess ammonia will overwhelm hepatic detoxification.

Result of ammonia overwhelming hepatic detoxification

Ruminal and systemic metabolic alkalosis and hyperammonemia.

Main neurotoxin in ammoniated feeds

Dialkylimidazoles - (imadazoles) inhibit the TCA cycle (think polio)

Onset of dz w/ Ammonia/Urea Toxicity

occurs rapidly w/in minutes to days of diet exposure.

Animals affected by Ammonia/Urea Toxicity (2)

Groups of animals.

Calves can develop dz by nursing from affected cows.

CS of Ammonia/Urea Toxicity (8)

Ataxia.

Bellowing.

Hyperexcitability.

Paddling.

Vocalization.

Bouts of mania.

Hyperesthesia.

Sawhorse stance at rest (some do this).

Tx for Ammonia/Urea Toxicity (3)

(Most animals die w/in hours)

Sedatives.

Rumen acidifiers - vinegar to decrease ammonia production/absorption.

Thiamine (looks like polio, don't only do this but won't hurt).

Vitamin A deficiency most commonly affects

growing feedlot cattole.

Vitamin A and its pre-cursor are plentiful in

green forage, but often deficient in cereal grains and stored feed (Destroyed by heat and time)

Vitamin A Deficiency leads to (3)

retinal atrophy.

narrowing of bony foramina of the skull.

decreased CSF absorption.

Vitamin A Deficiency calves CS (3)

ill thrift.

secondary infection.

peripheral blindness (can be central if occipital lobe is affected).

Adults w/ Vitamin A Deficiency: CS (3)

better condition, but more pronounced neuro signs.

Star-gazing.

peripheral blindness (negative PLR).

Peripheral blindness w/ Vitamin A Deficiency occur due to (3)

retinal atrophy.

papilledema.

compression of the optic nn.

Central blindess in Vitamin A Deficiency can occur due to

pressure necrosis of the occipital lobes

Calves born to Vitamin A Deficient moms may be delivered early and have birth defects including (3)

domed skull.

ocular defects.

thickened carpal jts.

Dx of Vitamin A Deficiency (6)

Dilated, non-responsive pupils.

Retinal atrophy.

Papilledema - enlargement and loss of color/detail in the optic disk.

Enlarged and torturous retinal vessels (once blocked by swollen disk).

+/- hemorrhage.

Low blood/feed Vitamin A levels.

CSF changes w/ Vitamin A Deficiency

Mononuclear pleocytsosis and an increase in protein (non-specific).

Tx for Vitamin A Deficiency (2)

Vitamin A IM in acute cases.

Diet enrichment.

Vitamin A Deficiency changes (general concept)

early change = reversible.

late changes = irreversible.

Focal/Multifocal Brain disorder often caused

asymmetric signs.

Forms of Listeriosis (3)

Septicemic (rare in ruminants).

local infection of the mammary glands or repro tract.

localized neuro form.

Sources of Listeria monocytogenes for ruminants (4)

alkaline silage (means its spoiled/oxygenated - most cases here are NOT silage).

Wooded pastures.

rotting vegetation.

feed contaminated w/ feces from shedding animals.

Listeria mechanism of transmission

organism invades through defects in the buccal mucosa and ascents roots of the CNs to the brain.

(may also see hematogenous spread).

Which CN root is mainly ascended by Listeria

Trigeminal

Once Listeria is in the brain

multifocal brainstem microabscesses lead to CS.

CS of Listeriosis (2)

Fever early in dz.

Focal or multifocal, unilateral Ca CN signs - CN 5-12.

Listeriosis: CN signs (7)

facial analgesia.

lip or ear droop.

absent palpebral response.

nystagmus.

head tilt.

circling.

dysphagia.

CSF results for listeriosis

mononuclear pleocytosis (even though it is bacterial), increased protein

CP abnormalities w/ Listeriosis

Electrolyte and acid base disturbances due to salivary losses.

Dx of Listeriosis (3)

CS and Hx of possible exposure.

CSF.

Culture of organism from feed, CSF, or lesion.

Tx for Listeriosis - ABX options

Tetracycline - better brain penetration.

High dose Penicillin.

Tx duration for Listeriosis

Minimum of 7d, preferably 14-28d.

Prognosis for Listeriosis

based on duration and severity of infection.

Microscopic lesions for Listeriosis

mononuclear perivacular cuffing.

neutrophilic microabscesses in the brainstem (esp around CN 5, 7, 8, and 9)

Control for Listeriosis (2)

Decrease exposure.

Vxn - not available in US.

Brain abscesses usually start

hematogenous that goes extradural (pituitary, sinus, and bone) and cause compression of adjacent brain tissue.

CS for brain abscess (3)

Slow to develop.

Unilateral blindness.

If mass affects hypothalamus or brainstem can see Bradycardia.

Most common isolate from brain abscess

Older - Truperella.

younder - Fusobacterium.

Tx for brain abscess

Long term ABX (see meningitis Tx).

Prognosis for brain abscesses

poor

Otitis media-interna is an

occasional sequala to bacterial resp infection in ruminants. Infection ascends the Eustachian tube.

Otitis media-interna: Most common type of cattle affected (2)

feedlot cattle and lambs at highest risk (due to association w/ resp dz.

dairy calves on Mycoplasma mastitic milk.

Otitis media-interna CS (3)

Vestibular signs

ipsilateral facial n. paralysis.

if cerebellum involvement can see paradoxic signs - circle and tilt in other direction.

Dx of Otitis media-interna (3)

otoscopic exam - TM usually ruptured in calves, although not always in sheep.

CS.

Aspirates.

Ddx for Otitis media-interna

Listeriosis.

Tx for Otitis media-interna

Long course, systemic ABX - 2-3wks (same as those used for resp dz).

Otitis media-interna: Even after tx

residual CN deficits may remain.